Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen reports have identified an association between lower dietary calcium consumption and higher blood pressure in adults. The relationship between dietary calcium and blood pressure status of humans may be modified by a wide variety of demographic, environmental, life-style, and nutritional factors. Reduced dietary calcium intake may be a proximate cause of several of the reported biochemical abnormalities of Ca2+ metabolism including the reductions in serum ionized Ca2+ concentrations and increases in circulating parathyroid hormone levels. The paradoxical increases in intracellular free Ca2+ observed in hypertension on low dietary Ca2+ intake suggest that a primary defect in the cellular handling of Ca2+ may exist, possible mediated through defective Ca2+ adenosine triphosphatase pump activity.
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PMID:Epidemiological evidence associating dietary calcium and calcium metabolism with blood pressure. 295 Jul 55

The effect of parathyroid hormone on erythrocytes from newborn and adult rabbits was studied in relation to the fragility pattern in hypotonic salt solutions and the activities of Ca- and Mg-dependent ATPases. Median osmotic fragility of red blood cells from newborn rabbits was significantly higher than in red blood cells from mature rabbits. Parathyroid hormone increased the mean osmotic fragility of red blood cells from newborn and adult rabbits, but showed the greater effect on those from newborns. Similarly, the hormone stimulated to a much greater extent the Ca-ATPase, but not the Mg-ATPase in red blood cells from the newborn rabbits, in comparison with red blood cells from adult rabbits. Parathyroid hormone, which is greatly elevated in the blood of patients with chronic renal failure, may be one cause for the anaemia seen in these patients, and its effect, which is mediated by Ca-ATPase activity, is stronger on young red blood cells. Significant morphological changes in the young red blood cells, observed by scanning electron microscopy, were caused by parathyroid hormone.
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PMID:Effect of parathyroid hormone on the fragility and enzyme activities of red blood cells from young and mature rabbits. 295 52

The effect of parathyroid hormone at concentrations found in uremic patients on erythrocytes (RBC) from newborn and adult rabbits was studied in relation to the fragility pattern in hypotonic salt solutions and the activities of Ca- and Mg-dependent ATPases. Median osmotic fragility of RBC from newborn rabbits was significantly lower than in mature rabbits. Parathyroid hormone (PTH) stimulated to a greater extent the mean osmotic fragility in RBC from newborn rabbits, than in those from adults. Similarly, the hormone stimulated to a much greater extent the Ca-ATPase but not the Mg-ATPase in RBC from the newborn rabbits, in comparison to those from adult rabbits. PTH, which is greatly elevated in the blood of patients with chronic renal failure, may be one cause of the anemia seen in these patients, and its effect, which is mediated by Ca-ATPase activity, is stronger on young RBC. There were significant morphological changes in the young RBC caused by PTH, as seen with scanning electron microscopy.
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PMID:Biochemical changes associated with the osmotic fragility of young and mature erythrocytes caused by parathyroid hormone in relation to the uremic syndrome. 295 61

A high affinity, calmodulin-sensitive (Ca2 + Mg2+)-ATPase was demonstrated in the plasma membrane preparation of three different osteosarcoma cell lines previously demonstrated to respond to parathyroid hormone with an increase in cytosolic calcium and a decrease in pH. The maximal velocity of the enzyme activity in the membrane preparations ranged from 0.83 to 2.42 nmol Pi released per min per mg protein with half-saturation constants of 26 nM of free Ca. The enzyme activity was not affected by Na+, K+, ouabain and azide, and exhibited an absolute requirement for Mg2+ ions. These results suggest a possible role for a membrane Ca2 + Mg2+-ATPase in initiating and perpetuating the ionic control of osteoblastic function.
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PMID:Characterization of a (Ca2+ + Mg2+)-ATPase system in the osteoblast plasma membrane. 297 93

The proximal tubule is the target site for parathyroid hormone (PTH), and conversion of 25(OH)vitamin D3 hormones which impinge on calcium (Ca) homeostasis, as well as a major site for sodium (Na) reabsorption. The effect of changes in PTH and vitamin D status on Na,K-ATPase activity, as a measure of Na transport, were studied in the proximal tubules of adult rat kidneys where Na and Ca reabsorption rates are in parallel. Na,K-ATPase activity and 25(OH)D3 metabolism were determined in cortical and juxtamedullary proximal tubule segments from normal, parathyroidectomized (PTX), and vitamin D-deficient (-D) rats. Na,K-ATPase activity was highest in cortical segments. PTX led to a decrease in activity in convoluted segments but increased activity in straight segments. In -D rats, Na,K-ATPase activity decreased in cortical segments but increased in juxtamedullary segments. 25(OH)D3 was metabolized more to 24,25(OH)2D3 than to 1,25(OH)2D3 in all normal segments. Juxtamedullary segments were more sensitive to PTX and -D conditions. These findings suggest that cortical and juxtamedullary nephrons are inherently different in basal Na,K-ATPase activity, in conversion of 25(OH)D3 to active metabolites, and in response to altered PTH and vitamin D3 status.
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PMID:Na,K-ATPase activity and 25(OH)vitamin D3 hydroxylation in rat proximal tubules. 302 30

Renal proximal tubule cells adapt to dietary phosphate (Pi) restriction by increasing Pi transport independent of parathyroid hormone, vitamin D metabolites, or serum Ca2+. To determine the underlying cellular mechanism(s), brush border (BBM) and basolateral membranes (BLM) were isolated from growing male rats fed a synthetic diet containing variable levels of Pi (0.1-1.4%). Dietary Pi restriction was without effect on either BBM or BLM total lipid phosphorus, individual phospholipid species, or BLM Na+-K+-ATPase specific activity. However, dietary Pi restriction (0.1 vs. 1.0%) did cause a significant reduction in BBM but not BLM cholesterol (0.45 vs. 0.41 mumol/mg protein). Brush border membrane cholesterol was inversely correlated with the tubular reabsorption of Pi (r = 0.77, P less than 0.01) over a broad range (99.9-46.2%). Arrhenius analysis of two intrinsic BBM enzymes revealed a significant reduction in the breakpoint temperature for alkaline phosphatase but no change for Mg2+-ATPase. Fluorescence polarization studies showed increased BBM inner core fluidity due to an alteration in neutral lipids but not phospholipid, fatty acid, or protein membrane components. These data demonstrate that the BBM can regulate its cholesterol content independent of the BLM. Furthermore, they suggest that adaptation to dietary Pi restriction involves a reduction in BBM cholesterol, which may be mediated by an increase in membrane fluidity.
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PMID:Renal apical membrane cholesterol and fluidity in regulation of phosphate transport. 316 Feb 47

This study examined the effect of parathyroid hormone (PTH) on myocardial energy production, transfer, and utilization. Rats (150 to 200 g) were injected with 1-84 PTH, 200 U/day i.p., or 1-34 PTH, 200 or 300 U/day i.p., for 4 days. Control animals received the vehicle only. The effect of the simultaneous administration of calcium channel blocker, verapamil, was also examined. Myocardial contents of Pi, ATP, and CP were significantly (P less than 0.01) lower in the 1-84 PTH-treated rats than in control animals. Both 1-84 PTH and 1-34 significantly (P less than 0.01) reduced mitochondrial oxygen consumption without altering ADP:O ratio indicating reduced phosphorylation. 1-84 and 1-34 PTH significantly (P less than 0.01) reduced the activities of mitochondrial and myofibrillar creatine phosphokinase and 1-84 PTH inhibited (P less than 0.01) the activities of mitochondrial Mg ATPase and those of myofibrillar Ca ATPase. There were significant (P less than 0.01) increments in myocardial 45Ca and in total calcium content in 1-84 PTH-treated rats. Verapamil abolished all the effects of 1-84 PTH. Similarly, inactivation of 1-84 PTH abolished its effects. Treatment with 1-84 PTH for 10 days was associated with a significant decrease in cardiac index and mean arterial pressure. Our data demonstrate that both 1-84 and 1-34 PTH impair energy production, transfer, and utilization. These biochemical derangements, if maintained, produce a decrease in cardiac index. It appears that the enhanced entry and the accumulation of calcium in the myocardium, either directly and/or indirectly, are responsible for the action of PTH on energy metabolism of the heart.
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PMID:Effect of parathyroid hormone on myocardial energy metabolism in the rat. 316 Aug 82

In order to elucidate the mechanism of pregnancy-induced hypertension (PIH) from the point of view of vascular resistance, we measured the intracellular Na+ concentrations and the membrane Na+ effluxes using red blood cells from normal pregnant females and patients with PIH. We also discussed the influences of hormones such as estrogen, progesterone, dehydroepiandrosterone sulfate (DHAS), hydrocortisol, human placental lactogen (hPL), human chorionic gonadotropin (hCG), and prolactin and parathyroid hormone (PTH) on the membrane Na+ effluxes. The intracellular Na+ concentrations were lower and the Na+-K+-ATPase activities were slightly higher both in the luteal phase and in the first trimester of normal pregnancy than those in the follicular phase, after which the former gradually increased and the latter gradually decreased until term to the mean values of those in the whole menstrual period. In mild PIH, the intracellular Na+ concentrations were not significantly increased, and the Na+-K+-ATPase activities were significantly increased compared to those in the third trimester of normal pregnancy, which suggests the compensatory increase of the Na+-K+-ATPase activities as opposed to the increase of the intracellular Na+ concentrations. In severe PIH, the intracellular Na+ concentrations were significantly increased compared with those in the third trimester of normal pregnancy and slightly increased compared with those in mild PIH, whereas the Na+-K+-ATPase activities were slightly decreased compared with those in mild PIH, which indicates a breakdown of the compensatory increase of the Na+-K+-ATPase activities. The intracellular Na+ concentrations in PIH are significantly correlated to diastolic pressure, systolic pressure and mean blood pressure. When the male red blood cells were incubated with the hormone, dose-dependently the Na+-K+-ATPase activities were significantly elevated by hydrocortisol and slightly elevated by progesterone and hPL, and they were significantly depressed by estrogen and prolactin and slightly depressed by PTH. These results suggest that the peripheral vascular resistance might be increased in the third trimester of normal pregnancy compared with that in the first trimester because the intracellular Na+ concentrations were elevated, and the Na+-K+-ATPase activities in the cell membrane were decreased along the course of pregnancy as a result of the effects of various hormones in the maternal blood.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A study on the membrane Na+ efflux of pregnancy-induced hypertension (PIH)]. 320 19

Aging in industrialized societies is accompanied by increases in the incidence and prevalence of hypertension, with a disproportionately greater increase occurring among aging blacks than among aging whites. This geriatric hypertension is generally of a salt-sensitive nature with a disproportionate frequency of isolated systolic hypertension. Although salt-taste acuity declines with age, salt sensitivity among the elderly does not appear to result from a compensatory increase in salt intake. Rather, age-related increases in salt sensitivity result, in part, from a reduced ability to appropriately excrete a salt load, which is due to a decline in renal function and to a reduced generation of natriuretic substances such as prostaglandin E2 and dopamine. Age-associated declines in the activity of membrane sodium/potassium-adenosine triphosphatase (Na/K-ATPase) may also contribute to geriatric hypertension because this results in increased intracellular sodium that may cause reduced sodium-calcium exchange and thereby increase intracellular calcium and vascular resistance. Reductions in cellular calcium efflux due to reduced calcium-ATPase activity may similarly cause an increase in intracellular calcium and vascular resistance. Increasing dietary calcium intake may represent an effective nonpharmacologic treatment for some salt-sensitive persons because it appears to reduce intracellular calcium by (1) suppressing parathyroid hormone-mediated calcium influx, (2) increasing Na/K-ATPase activity, and (3) reducing intravascular volume due to calcium-induced natriuresis.
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PMID:Salt sensitivity and systemic hypertension in the elderly. 328 54

Excretion of acid (or generation of bicarbonate) by the kidneys is necessary for acid-base homeostasis. Most of this acid is excreted in the form of ammonia and titratable acid, the latter representing the amount of acid required to titrate the urine buffers from the plasma pH to urine pH. The transport of ammonia in the kidney is now recognized to entail more than simple nonionic diffusion of NH3 and trapping of NH4+. NH4+ transport in the kidney probably occurs by passive diffusion and by transport on the Na+-H+ exchanger, the Na+-K+-2Cl- transporter and on Na+-K+-ATPase. NH3 diffusion is stimulated by an acid disequilibrium pH in various nephron segments. Also, diffusion equilibrium of NH3 in various regions of the kidney has now been disproved. These various mechanisms of ammonia transport are considered in terms of their possible changes with acid-base disturbances. Phosphate is the most predominant urine buffer; its urinary excretion increases with acidosis. The mechanisms probably involve a decrease in the preferentially transported species, HPO4(2-), and a direct effect of pH on proximal tubule apical phosphate transport. With chronic acidosis, changes in the activity of the apical Na+-phosphate transporter occur. These effects of systemic acid-base balance interact with parathyroid hormone and dietary phosphate status to alter phosphate reabsorption. Citrate transport in the kidney is analyzed because of its sensitivity to systemic pH and because of the possible influence on systemic acid-base status in certain circumstances. Alterations in citrate excretion with acid-base disturbances depend on changes in the concentration of the transported species, citrate2-, and on changes in renal metabolism.
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PMID:Roles and mechanisms of urinary buffer excretion. 331 Jun 62


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